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压力感受器去神经支配对无肾犬容量负荷性高血压的影响。

Effects of baroreceptor denervation on volume loading hypertension in anephric dogs.

作者信息

Manning R D, Cowley A W, Coleman T G

出版信息

Hypertension. 1985 Jul-Aug;7(4):562-8. doi: 10.1161/01.hyp.7.4.562.

DOI:10.1161/01.hyp.7.4.562
PMID:4007991
Abstract

The role of the baroreceptor mechanism in determining the relationship between fluid volume and arterial pressure is not clear. Therefore, the effects of the baroreflex on the arterial pressure and fluid volume of conscious, anephric dogs were studied after a sustained 10% increase in blood volume. The animals were equipped with long-term indwelling arterial and venous catheters, and arterial pressure was monitored 24 hours a day. The increase in blood volume was achieved by intravenous infusion of 50 ml/kg of lactated Ringer's solution in 30 minutes. After volume loading arterial pressure increased rapidly to hypertensive levels (130.8 +/- 7.5% of control) in a baroreceptor denervated group. The initial increase in arterial pressure in a group of normally innervated dogs was smaller (118.8 +/- 1.8% of control), but by 24 hours postinfusion the arterial pressure of both groups had reached the same level. The innervated group had probably experienced baroreceptor resetting by this time. Blood volume both before and after infusion was not different in the denervated and innervated groups; however, sodium space was markedly higher before the infusion in the denervated dogs (431.8 +/- 13.8 ml/kg vs 344.8 +/- 19.0 ml/kg in the innervated dogs), and the volume load caused parallel increases in this space in the denervated and innervated groups. The present study shows that the blood volume of anephric dogs was unchanged after baroreceptor denervation while the extracellular fluid volume of denervated dogs was elevated. Furthermore, a small sustained increase in blood volume in either conscious, innervated dogs or conscious, baroreceptor denervated dogs, in contradistinction to the effects in anesthetized dogs, resulted in significant increases in arterial pressure (p less than 0.05).

摘要

压力感受器机制在决定体液容量与动脉血压之间关系中的作用尚不清楚。因此,在血容量持续增加10%后,研究了压力反射对清醒无肾犬动脉血压和体液容量的影响。给这些动物安装了长期留置的动脉和静脉导管,每天24小时监测动脉血压。通过在30分钟内静脉输注50 ml/kg的乳酸林格氏液来实现血容量的增加。在压力感受器去神经支配组中,容量负荷后动脉血压迅速升高至高血压水平(为对照值的130.8±7.5%)。一组正常支配犬的动脉血压初始升高较小(为对照值的118.8±1.8%),但在输注后24小时,两组的动脉血压达到相同水平。此时,支配组可能已经经历了压力感受器重调定。去神经支配组和支配组在输注前后的血容量没有差异;然而,去神经支配犬在输注前的钠间隙明显更高(431.8±13.8 ml/kg,而支配犬为344.8±19.0 ml/kg),容量负荷使去神经支配组和支配组的该间隙平行增加。本研究表明,压力感受器去神经支配后无肾犬的血容量未改变,而去神经支配犬的细胞外液容量升高。此外,与麻醉犬的情况不同,清醒支配犬或清醒压力感受器去神经支配犬血容量的小幅持续增加导致动脉血压显著升高(p<0.05)。

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